The human eye is capable of both day and night vision. Rod cells, or rods, are photoreceptor cells in the retina of the eye that can function in less intense light than can the other type of photoreceptor, cone cells. Being more light sensitive, rods are responsible for night vision. Named for their cylindrical shape, rods are concentrated in all parts of the retina except its center and thus provide peripheral vision. Cone cells, or to cones, are photoreceptor cells in the center of the retina of the eye which function best in relatively bright light. The cone cells gradually become sparser towards the periphery of the retina.
Diseases of the eye may affect one type of vision or the other or both. In certain diseases, first night vision is affected, while day vision is affected as the disease progresses.
Retinitis pigmentosa (RP) comprises a group of relatively common inherited diseases characterized by progressive degeneration of the retina of the eye. The continually spreading destruction of the retina leads to increasingly severe visual loss. Vision gradually degenerates from the periphery [night vision, wide visual field] to the center [high definition day vision, colors]. Symptoms start with a decrease in dark adaptation leading to night blindness. There is a simultaneous reduction in the peripheral field of view up to tunnel vision. Central (day) vision is subsequently lost leading to total blindness. The rate of progression of RP varies according to the specific genetic defect. The visual impairment problem is much more prevalent than blindness.
Currently, no treatment is recognized to improve the vision of RP patients. Vitamin A palmitate (15,000 U/d) is prescribed to slow the progress of RP by about 2% per year. Current clinical trials are underway to attempt to slow degeneration, and include:
Ciliary Neurotrophic Factor eye Implant
Omega 3 amino acid (DHA)
Lutein (10 or 30 mg/day) capsules
Vitamin A
Vitamin E
Over the last 15 years, researchers have pinpointed defects in dozens of genes causing different forms of RP. Surprisingly, in some cases, patients with the same genetic defect can show different severities of vision loss and rates of disease progression. This effect is most dramatic across the retina of some individuals where regions with normal vision can abut regions of no vision. Environmental factors have been near the top of the suspect list for this variation in severity. An environmental factor experienced by all, but to varying extents, is exposure to light bright lights have been previously speculated to accelerate certain forms of RP.
About 100 mutations in the rhodopsin gene have been shown to cause RP but understanding of the steps between mutant proteins and death of rod photoreceptors remains incomplete. Many of the patients with rhodopsin mutation are known to have better prognosis while other suffer from blindness since early childhood with rapid degeneration.
Another eye disease is Leber's congenital amaurosis (LCA). RP and LCA are not the same disease although a few of the genes are common.
A large majority of blindness and low vision in developed countries is due to Age Related Macular Degeneration (AMD), a disease which involves destruction of the photoreceptors. AMD affects more than 1.75 million individuals in the United States. Owing to the rapid aging of the US population, this number will increase to almost 3 million by 2020 (Arch Ophthalmol. 2004; 122:564).
Night blindness also occurs in non-degenerative eye diseases. Examples of such diseases include congenital night vision disorder, congenital stationary night blindness, fundus albipunctatus and vitamin A deprivation syndrome. Congenital stationary night blindness is an inherited eye disorder that principally affects the rod photoreceptors in the retina, impairing night vision. There may also be moderate to high myopia (short sightedness). Under good lighting conditions, there is usually no visual deficit. There are several different types of the disorder which are inherited in an autosomal dominant, autosomal recessive, or X-linked recessive manner. The X-linked type affects almost exclusively males and accounts for the predominance of males with congenital stationary night blindness.
WO 2007/109824 discloses a process for preparing a stable packaged dosage form comprising an oxidation-sensitive material such as carotenes and carotenoids in whole dried algae of the genus Dunaliella. The dosage form is described as being useful to in the treatment of a plurality of diseases including optical disorders such as macular degeneration or cataracts.
J. Preston Van Hooser, Tomas S. Aleman, Yu-Guang He, Artur V. Cideciyan, Vladimir Kuksa, Steven J. Pittler, Edwin M. Stone, Samuel G. Jacobson, Krzysztof Palczewski (2000) Rapid restoration of visual pigment and function with oral retinoid in a mouse model of childhood blindness. PNAS, vol. 97 no. 15, 8623-8628, analyzed retinoid flow in Rpe65-deficient mice, a model of Leber congenital amaurosis, which have no rod photopigment and severely impaired rod physiology. They intervened by using oral 9-cis-retinal, attempting to bypass the biochemical block caused by the genetic abnormality. Within 48 h, there was formation of rod photopigment and dramatic improvement in rod physiology.
J. Preston Van Hooser, Yan Liang, Tadao Maeda, Vladimir Kuksa, Geeng-Fu Jang, Yu-Guang He, Fred Rieke, Henry K. W. Fong, Peter B. Detwiler, and Krzysztof Palczewski (2002) Recovery of Visual Functions in a Mouse Model of Leber Congenital Amaurosis. J. Biol. Chem., Vol. 277, Issue 21, 19173-19182, provide evidence that early intervention by 9-cis-retinal administration significantly attenuated retinal ester accumulation and supported rod retinal function for more than 6 months post-treatment. In single cell recordings rod light sensitivity was shown to be a function of the amount of regenerated isorhodopsin; high doses restored rod responses with normal sensitivity and kinetics.
Syed M. Noorwez, Ritu Malhotra, J. Hugh McDowell, Karen A. Smith, Mark P. Krebs|, and Shalesh Kaushal (2004) Retinoids Assist the Cellular Folding of the Autosomal Dominant Retinitis Pigmentosa Opsin Mutant P23H. J. Biol. Chem., Vol. 279, Issue 16, 16278-16284, demonstrate that the mutant opsin P23H, associated with autosomal dominant retinitis pigmentosa, is effectively rescued by 9- or 11-cis-retinal, the native chromophore. P23H rhodopsins containing 9- or 11-cis-retinal had blue-shifted absorption maxima and altered photo-bleaching properties compared with the corresponding wild-type proteins.
There is no description in the scientific literature of a treatment causing an improvement in day vision of an RP patient.